It has been determined that during the early phases of chemotherapy with 5-azacytidine, under conditions where resistance develops, there is an initial marked increase in an embryonic form of uridine kinase in rapidly growing mouse or rat tumors, with little change, or a decrease in the adult form. During the later stages of the development of resistance this total activity drops to near zero. Similarly, during the early phases of chemotherapy with corticosteroids, there appears to be an increase in the corticosteroid-binding protein in the tumor cells. The work on the fluctuations in uridine kinases will be extended to other pyrimidine analogs which are both cancer chemotherapeutic agents and which are activated by uridine kinase. Attempts will be made to achieve a complete separation of the uridine kinase isozymes preliminary to a kinetic analysis of the 2 isozymes using the normal substrates and the analogs. A similar approach will be applied to the corticosteroid- binding proteins. The results of such studies have definite predictive value in chemotherapy, which may be utilized in postponing the development of resistance; this is particularly true if the two isozymes or binding proteins exhibit a differential affinity for the normal substrates and analogs.